MRSA: Tracing the Roots of Antibiotic Resistance

ST398 started out as an antibiotic-sensitive bacterium in humans. After it spread to livestock, antibiotic resistance began.

The idea that feeding antibiotics to farm animals can fuel antibiotic resistance in bacteria that cause human disease is not just theory, it has already happened. A recent genetic analysis of one increasingly troublesome strain of MRSA reveals that it almost certainly started out in humans as a non-resistant strain, and then jumped to pigs, where it acquired resistance to methicillin and tetracycline as a result of the presence of these antibiotics in animal feed. These bacteria now infect both humans and animals.

ST398 started out as an antibiotic-sensitive bacterium whose natural host was humans. It was only after it spread to livestock that antibiotic resistance began to appear.

In 2003, a novel form of methicillin-resistant Staphylococcus aureus, the notorious MRSA superbug, called ST398 began to emerge in livestock and soon began infecting farm workers. It is estimated that in some regions of the Netherlands, ST398 accounts for 25 to 35% of all human MRSA cases and 12% of all cases in the entire country. But until now, it was presumed that pigs and/or other animals were the natural hosts of ST398.

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It is possible to trace the evolutionary history of a bacterial strain backwards in time by doing a thorough genetic analysis of its subtypes and looking closely at the differences in mutations between individual subtypes. This can reveal which mutations are newer and which are more ancient.

Researchers from several institutions recently did such an analysis on 89 different isolates of ST398 from 19 countries spanning four continents. These isolates came from humans and animals and included both antibiotic-resistant and sensitive subtypes. The evolutionary tree that emerged showed that the most ancient of these bacteria were antibiotic-sensitive isolates from humans. These are almost certainly the forerunners of all the other bacterial isolates.

In other words, ST398 started out as an antibiotic-sensitive bacterium whose natural host was humans. It was only after it spread to livestock that antibiotic resistance began to appear in these bacteria.

Feeding antibiotics to meat animals leads to an increase in the animals' weight and makes meat less expensive to produce. But concerns that this practice causes a widespread increase in bacterial antibiotic resistance led the European Union to ban the feeding of all medically important antibiotics to livestock in 1998 and extend the ban to all antibiotics in 2006.

In the U.S., routine administration of antibiotics to livestock raised for meat remains standard practice. The U.S. has banned the use of certain antibiotics in poultry (fluoroquinolones such as Cipro) and has recently limited the use of one other class of antibiotic in livestock (cephalosporins). This still leaves many other antibiotics that can be and are routinely fed to livestock.

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A 2001 study estimated that 24.6 million pounds of antibiotics are fed to livestock in the U.S. for non-therapeutic purposes every year, more than twice the amount used by humans. There's little evidence that these numbers have changed much over the past decade.

The current study offers some hard evidence that this practice is not in the best interest of public health.

An article on the genetic analysis of ST398 was published online by mBio.